Multimodality MR Imaging Findings of Low-Grade Brain Edema in Hepatic Encephalopathy

Zhang, L.J.; Zhong, Jianhui; Lu, Guang Ming

doi:10.3174/ajnr.a2968

Cited by 40 publications

(33 citation statements)

References 41 publications

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“…The presence of diffusion restriction most strongly suggests arterial stroke, toxicity, infection, or, to a lesser degree, lymphoma or deep venous thrombosis. 1,2,4, [25][26][27]35,39,42,45,50,57,60,70,90 Conversely, diffusion restriction has not been found in patients with dAVF-induced thalamic dementia. Strong gadolinium enhancement is most consistent with a high-grade neoplasm; 26,27,58 however, other conditions including dAVFs can also have some degree of gadolinium enhancement.…”

Section: Thalamic Dementia Syndrome: Differential Diagnosis and Workupmentioning

confidence: 99%

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Holekamp

Mollman

Murphy

et al. 2016

JNS

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Nonhemorrhagic neurological deficits are underrecognized symptoms of intracranial dural arteriovenous fistulas (dAVFs) having cortical venous drainage. These symptoms are the consequence of cortical venous hypertension and portend a clinical course with increased risk of neurological morbidity and mortality. One rarely documented and easily misinterpreted type of nonhemorrhagic neurological deficit is progressive dementia, which can result from venous hypertension in the cortex or in bilateral thalami. The latter, which is due to dAVF drainage into the deep venous system, is the less common of these 2 dementia syndromes. Herein, the authors report 4 cases of dAVF with venous drainage into the vein of Galen causing bithalamic edema and rapidly progressive dementia. Two patients were treated successfully with endovascular embolization, and the other 2 patients were treated successfully with endovascular embolization followed by surgery. The radiographic abnormalities and presenting symptoms rapidly resolved after dAVF obliteration in all 4 cases. Detailed descriptions of these 4 cases are presented along with a critical review of 15 previously reported cases. In our analysis of these 19 published cases, the following were emphasized: 1) the clinical and radiographic differences between dAVF-induced thalamic versus cortical dementia syndromes; 2) the differential diagnosis and necessary radiographic workup for patients presenting with a rapidly progressive thalamic dementia syndrome; 3) the frequency at which delays in diagnosis occurred and potentially dangerous and avoidable diagnostic procedures were used; and 4) the rapidity and completeness of symptom resolution following dAVF treatment.http://thejns.org/doi/abs/10.3171/2015.5.JNS15473Key words dural arteriovenous fistula; cortical venous hypertension; thalamic edema; nonhemorrhagic neurological deficit; thalamic dementia; vascular disorders ©AANS, 2016 davF-induced thalamic dementiaBorden-Shucart classification system-based not only on angiographic appearance but also mode of presentationto permit more accurate risk stratification and assist with clinical decision making for the type and timing of dAVF treatment (Table 1). 68,91One relatively underappreciated type of NHND is progressive dementia resulting from dAVF-induced cortical venous hypertension, though correct diagnosis and treatment is increasing, thanks to improved imaging techniques.18,79 Dural AVF-induced progressive dementia can be differentiated as either cortical or thalamic in origin-2 categories that have relatively distinct patterns of clinical symptomatology 18,54,62,80,85 and highly specific venous outflow patterns.18,80 Of the two, dAVFinduced thalamic dementia is less frequent, with only 15 published cases reported in the literature to date. All were individual case reports, and several lacked adequate clinical, radiographic, and/or treatment specifics to permit detailed assessment as to manner of presentation, underlying hemodynamic pathophysiology, and long-term outcome. 18,[21][22][23]...

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Section: Thalamic Dementia Syndrome: Differential Diagnosis and Workupmentioning

confidence: 99%

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Holekamp

Mollman

Murphy

et al. 2016

JNS

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“…To maintain osmotic equilibrium, astrocytes export osmolytes such as mIns and Cho (decreased mIns/Cr and Cho/Cr on 1 H-MRS) (Zhang et al 2013). These 1 H-MRS findings were seen in all examined brain regions of HE patients compared with controls Zhang et al 2013). Patients infected with HCV showed elevated Cho, Cr, and mIns compared to healthy controls and those with hepatitis B, which may be due to microglial activation.…”

Section: General Application By Mr Imaging Of Neuroinflammation In Hementioning

confidence: 92%

“…Glutamine (increased Glx/Cr on 1 H-MRS) increased intracellular osmolality. To maintain osmotic equilibrium, astrocytes export osmolytes such as mIns and Cho (decreased mIns/Cr and Cho/Cr on 1 H-MRS) (Zhang et al 2013). These 1 H-MRS findings were seen in all examined brain regions of HE patients compared with controls Zhang et al 2013).…”

Section: General Application By Mr Imaging Of Neuroinflammation In Hementioning

confidence: 93%

“…HE has typical 1 H-MRS findings, i.e., lower Cho/Creatine (Cr) and mIns/Cr as well as higher glutamine/glutamate (Glx)/ Cr (Fig. 5) compared with healthy controls (Zhang et al 2013). mIns and Cr are putative glial markers.…”

Section: General Application By Mr Imaging Of Neuroinflammation In Hementioning

confidence: 98%

“…The diagnostic accuracy of psychometric tests is limited (Kircheis et al 2014). Therefore, it is beneficial to develop qualitative and quantitative methods such as imaging biomarkers to diagnose HE (Zhang et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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PET and MR imaging of neuroinflammation in hepatic encephalopathy

Yang

et al. 2014

Metab Brain Dis

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Neurological or psychiatric abnormalities associated with hepatic encephalopathy (HE) range from subclinical findings to coma. HE is commonly accompanied with the accumulation of toxic substances in bloodstream. The toxicity effect of hyperammonemia on astrocyte, such as the alteration in neurotransmission, oxidative stress, astrocyte swelling, is considered as an important factor in the pathogenesis of HE. Besides, neuroinflammation has captured more attention in the process of HE, but the mechanism of neuroinflammation leading to HE remains unclear. Molecular imaging techniques such as positron emission tomography (PET) and magnetic resonance imaging (MRI) targeting activated microglia and/ or other mediators appear to be promising noninvasive approaches to assess HE. This review focuses on novel imaging and therapy strategies of neuroinflammation in HE.

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The effect of rifaximin and lactulose treatments to chronic hepatic encephalopathy rats: An [¹⁸F]PBR146 in‐vivo neuroinflammation imaging study

Kong,

Luo,

et al. 2024

Brain and Behavior

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IntroductionHepatic encephalopathy (HE) is a severe neuropsychiatric complication of liver diseases characterized by neuroinflammation. The efficacies of nonabsorbable rifaximin (RIF) and lactulose (LAC) have been well documented in the treatment of HE. [18F]PBR146 is a translocator protein (TSPO) radiotracer used for in vivo neuroinflammation imaging. This study investigated anti‐neuroinflammation effect of RIF or/and LAC in chronic HE rats by [18F]PBR146 micro‐PET/CT.MethodsBile duct ligation (BDL) operation induced chronic HE models, and this study included Sham+normal saline (NS), BDL+NS, BDL+RIF, BDL+LAC, and BDL+RIF+LAC groups. Behavioral assessment was performed to analyze the motor function, and fecal samples were collected after successfully established the chronic HE model (more than 28 days post‐surgery). In addition, fecal samples collection and micro‐PET/CT scans were performed sequentially. And we also collected the blood plasma, liver, intestinal, and brain samples after sacrificing the rats for further biochemical and pathological analyses.ResultsThe RIF‐ and/or LAC‐treated BDL rats showed similar behavioral results with Sham+NS group, while the treatment could not reverse the biliary obstruction resulting in sustained liver injury. The RIF or/and LAC treatments can inhibit IFN‐γ and IL‐10 productions. The global brain uptake values of [18F]PBR146 in BDL+NS group was significantly higher than other groups (p < .0001). The brain regions analysis showed that the basal ganglia, hippocampus, and cingulate cortex had radiotracer uptake differences among groups (all p < .05), which were consistent with the brain immunohistochemistry results. Sham+NS group was mainly enriched in Christensenella, Coprobacillus, and Pseudoflavonifractor. BDL+NS group was mainly enriched in Barnesiella, Alloprevotella, Enterococcus, and Enterorhabdus. BDL+RIF+LAC group was enriched in Parabacteroides, Bacteroides, Allobaculum, Bifidobacterium, and Parasutterella.ConclusionsRIF or/and LAC had anti‐neuroinflammation in BDL‐induced chronic HE rats with gut microbiota alterations. The [18F]PBR146 could be used for monitoring RIF or/and LAC treatment efficacy of chronic HE rats.

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Multimodality MR Imaging Findings of Low-Grade Brain Edema in Hepatic Encephalopathy

Cited by 40 publications

References 41 publications

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

PET and MR imaging of neuroinflammation in hepatic encephalopathy

The effect of rifaximin and lactulose treatments to chronic hepatic encephalopathy rats: An [¹⁸F]PBR146 in‐vivo neuroinflammation imaging study

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Multimodality MR Imaging Findings of Low-Grade Brain Edema in Hepatic Encephalopathy

Cited by 40 publications

References 41 publications

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

PET and MR imaging of neuroinflammation in hepatic encephalopathy

The effect of rifaximin and lactulose treatments to chronic hepatic encephalopathy rats: An [18F]PBR146 in‐vivo neuroinflammation imaging study

Contact Info

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The effect of rifaximin and lactulose treatments to chronic hepatic encephalopathy rats: An [¹⁸F]PBR146 in‐vivo neuroinflammation imaging study